摘要翻译：
细胞周期是一系列有序的事件，最终导致单个细胞分裂成两个子细胞。在DNA被辐射或化学物质损伤的情况下，细胞周期的$G_1}和$G_2}$阶段的损伤检查点被激活。这会导致细胞周期的停滞，从而使DNA损伤得以修复。一旦这样做，细胞继续其通常的活动周期。我们研究了在$G2期DNA损伤检查点的数学模型，它阻止了细胞周期从$G2期向$M期（有丝分裂期）的转变。肿瘤抑制蛋白p53在激活哺乳动物细胞周期阻滞通路中起着关键作用。如果DNA损伤严重，p53蛋白会激活其他导致细胞凋亡的途径，即程序性细胞死亡。p53基因的缺失导致含有受损DNA的细胞的增殖，即肿瘤的生长，最终可能变成癌变。最近的一些实验证据表明，p53基因的单个拷贝（在正常细胞中，每个基因有两个相同的拷贝）的突变足以引发肿瘤的形成。我们研究了减少p53和其他两个基因拷贝数对细胞周期阻滞的影响，并获得了与实验观察相一致的结果。
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英文标题：
《Gene Copy Number and Cell Cycle Arrest》
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作者：
Bhaswar Ghosh and Indrani Bose
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最新提交年份：
2005
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分类信息：

一级分类：Quantitative Biology        数量生物学
二级分类：Molecular Networks        分子网络
分类描述：Gene regulation, signal transduction, proteomics, metabolomics, gene and enzymatic networks
基因调控、信号转导、蛋白质组学、代谢组学、基因和酶网络
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一级分类：Quantitative Biology        数量生物学
二级分类：Other Quantitative Biology        其他定量生物学
分类描述：Work in quantitative biology that does not fit into the other q-bio classifications
不适合其他q-bio分类的定量生物学工作
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英文摘要：
  The cell cycle is an orderly sequence of events which ultimately lead to the division of a single cell into two daughter cells. In the case of DNA damage by radiation or chemicals, the damage checkpoints in the $G_{1}$ and $G_{2}$ phases of the cell cycle are activated. This results in an arrest of the cell cycle so that the DNA damage can be repaired. Once this is done, the cell continues with its usual cycle of activity. We study a mathematical model of the DNA damage checkpoint in the $G_{2}$ phase which arrests the transition from the $G_{2}$ to the $M$ (mitotic) phase of the cell cycle. The tumor suppressor protein p53 plays a key role in activating the pathways leading to cell cycle arrest in mammalian systems. If the DNA damage is severe, the p53 proteins activate other pathways which bring about apoptosis, i.e., programmed cell death. Loss of the p53 gene results in the proliferation of cells containing damaged DNA, i.e., in the growth of tumors which may ultimately become cancerous. There is some recent experimental evidence which suggests that the mutation of a single copy of the p53 gene (in the normal cell each gene has two identical copies) is sufficient to trigger the formation of tumors. We study the effect of reducing the gene copy number of the p53 and two other genes on cell cycle arrest and obtain results consistent with experimental observations.
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PDF链接：
https://arxiv.org/pdf/q-bio/0510012